Osler-Rendu-Weber disease, or hereditary hemorrhagic telangiectasia (HHT), is an autosomal dominant condition causing recurrent epistaxis, telangiectases and visceral vascular anomalies. It is caused by a mutation in either endoglin (located on human chromosome 9), activin receptor-like kinase 1 (on chromosome 12) or an as yet unidentified third gene. Common sources of serious morbidity in HHT are pulmonary vascular arteriovenous malformation (PAVM), cerebral arteriovenous malformation (CAVM) and hepatic arteriovenous malformation (HAVM). This study seeks to investigate six issues: 1) the prevalence of PAVMs in a population with HHT due to endoglin mutations; 2) the relative sensitivity and specificity of pulse oximetry, helical CT and contrast echocardiography as screening modalities for PAVMs; 3) the incidence of CAVMs in a population with HHT due to endoglin mutations; 4) the incidence of HAVM in a population with HHT due to endoglin mutations; 5) the existence of modifier genes that determine which individuals with endoglin mutations develop PAVMs, CAVMs, or HAVMs; and 6) the prevalence of abnormalities of the cardiac valves in those with endoglin mutations. We are continuing to enroll subjects in this protocol. Formal data analysis awaits enrollment of more individuals.